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61,005 resultsShowing papers similar to Inhaled Microplastics Inhibit Tissue Maintenance Functions of Pulmonary Macrophages
ClearDetrimental effects of microplastic exposure on normal and asthmatic pulmonary physiology
Researchers exposed both healthy and asthmatic mice to airborne microplastics and found significant lung inflammation, immune activation, and increased mucus production in both groups. Microplastic particles were taken up by immune cells called macrophages, and gene analysis revealed changes in immune response, cellular stress, and cell death pathways. The study suggests that inhaling microplastics may worsen respiratory health in both normal and vulnerable populations.
Alveolar macrophages promote lung organoid outgrowth but do not protect against negative effects of PA6,6 microplastics on developing airway organoids
Researchers added alveolar macrophages to developing airway organoids to test whether these immune cells protect lung tissue from the harmful effects of polyamide 6,6 microplastics. Macrophages promoted organoid growth but failed to shield airway cells from microplastic-induced damage, with leaching chemicals rather than the particles themselves being responsible for toxicity.
Inhaled microplastics and lung health: Immunopathological effects and disease implications
This review examines the molecular mechanisms by which inhaled microplastics damage lung health, focusing on oxidative stress, inflammation, and immune disruption. Researchers found that microplastics trigger reactive oxygen species production, deplete antioxidants, impair mitochondrial function, and compromise immune defenses in lung tissue. The evidence indicates that microplastics may also act as carriers for other toxic pollutants, amplifying respiratory health risks.
Polystyrene microplastics induce an immunometabolic active state in macrophages
Researchers found that polystyrene microplastics taken up by macrophages — immune cells lining the gut and lungs — triggered a metabolic shift toward an inflammatory state. This finding suggests microplastics reaching human tissues may alter immune function in ways that could contribute to inflammation-related diseases.
Impact of Microplastic Exposure on Airway Inflammation in an Acute Asthma Murine Model
Mouse experiments found that microplastic exposure worsened inflammatory responses in healthy lungs but did not further aggravate airway inflammation in mice with pre-existing asthma, suggesting the lung's response to microplastics depends on baseline immune state.
Microplastic-Induced Macrophage Dysfunction Drives Lung Tumor Progression through Glutathione Imbalance
Researchers found that microplastics trigger a cascade of immune dysfunction in macrophages through toll-like receptor signaling, leading to disrupted glutathione metabolism and macrophage cell death via ferroptosis. In tumor-bearing mice, orally ingested microplastics accumulated in the lungs and remodeled the immune microenvironment over time, with increased infiltration of inflammatory macrophages and impaired lymphocyte function accompanying greater tumor burden.
Microplastics and Nanoplastics Impair the Biophysical Function of Pulmonary Surfactant by Forming Heteroaggregates at the Alveolar–Capillary Interface
Scientists found that micro and nanoplastics from common products like foam packaging, lunch boxes, and water bottles can impair the function of pulmonary surfactant, the crucial substance that keeps our lungs from collapsing. Polystyrene foam particles caused the most damage, both in lab tests and in mice, where they triggered lung inflammation. The nanoplastic fraction, though a small part of the total mass, appeared to drive most of the harm by forming clumps with the surfactant at the air-liquid surface in the lungs.
Deleterious effects of microplastics and nanoplastics on rodent lungs: a systematic review
This systematic review summarizes research on how inhaled micro- and nanoplastics affect the lungs in animal studies. The findings show these particles can cause lung inflammation, tissue damage, and immune responses, suggesting that breathing in airborne microplastics may pose real risks to respiratory health.
Microplastics exposed by respiratory tract and exacerbation of community-acquired pneumonia: The potential influences of respiratory microbiota and inflammatory factors
Researchers found that microplastics were present in the lungs of pneumonia patients, and that patients with severe pneumonia had higher levels of microplastics in their airways than those with milder cases. The microplastics appeared to worsen lung infections by disrupting the balance of airway bacteria and increasing inflammation. This study provides early evidence that inhaled microplastics may make respiratory infections more dangerous in humans.
Interactions between inhalable aged microplastics and lung surfactant: Potential pulmonary health risks
Researchers examined how aged microplastics that have been weathered in the environment interact with lung surfactant, the thin liquid layer that lines the airways and aids breathing. They found that aged microplastics disrupted surfactant function more severely than pristine particles, potentially impairing the lungs' ability to expand and protect against inhaled pollutants. The study suggests that the weathering process makes airborne microplastics more hazardous to respiratory health over time.
Polystyrene microplastic particles: In vitro pulmonary toxicity assessment
Researchers tested the effects of polystyrene microplastics on human lung cells in the laboratory and found that the particles triggered inflammation and oxidative stress. The microplastics also weakened the protective barrier function of lung tissue by depleting key structural proteins. The study suggests that inhaling microplastics may increase the risk of respiratory problems by damaging the lung's natural defenses.
Microplastics inhalation: evidence in human lung tissue
Microplastic particles were found in human lung tissue samples collected during surgery, confirming that people inhale and retain microplastics in pulmonary tissue, with polypropylene and polyethylene terephthalate among the polymers identified, raising concerns about chronic respiratory and inflammatory effects.
Presence of airborne microplastics in human lung tissue
Researchers examined human lung tissue from autopsies and found microplastic particles and fibers in 13 out of 20 samples. The most common plastics were polyethylene and polypropylene, with particles smaller than 5.5 micrometers. This study provides direct evidence that inhaled microplastics accumulate in human lungs, raising concerns about potential long-term effects on respiratory health.
Chronic lung tissue deposition of inhaled polyethylene microplastics may lead to fibrotic lesions
In a mouse study, inhaled polyethylene microplastics accumulated in lung tissue over 90 days of repeated exposure, causing chronic inflammation, immune changes, and early signs of lung scarring (fibrosis). Even at the lowest doses, the microplastics triggered inflammatory cell buildup and thickening of lung walls. These findings suggest that long-term breathing of airborne microplastics could lead to permanent lung damage, which is concerning given rising levels of plastic particles in indoor and outdoor air.
Inhaled polystyrene microplastics impaired lung function through pulmonary flora/TLR4-mediated iron homeostasis imbalance
Mice that inhaled polystyrene microplastics for 60 days developed lung scarring, reduced lung function, and weakened lung barriers. The microplastics increased harmful bacteria in the lungs, which triggered an iron-related cell death process called ferroptosis -- revealing a new mechanism by which breathing in microplastics could cause lasting lung damage.
Microplastics, potential threat to patients with lung diseases
This review examines the potential threat that airborne microplastics pose to people with existing lung conditions, noting that these particles have been found in human lung tissue and sputum. Researchers explored possible mechanisms by which inhaled microplastics could worsen lung diseases, including triggering inflammation and oxidative stress. The study highlights significant knowledge gaps and calls for more research into how microplastic inhalation affects respiratory health.
Breathing plastics: Influence of airborne microplastics on the respiratory microbiome and health of human lungs (Review)
Researchers reviewed evidence showing that inhaled airborne microplastics can physically interact with the microbial community living in human lungs, disrupting its balance and triggering inflammation linked to conditions like asthma and fibrosis. Because microplastic particles have been found in lung tissue and fluid samples, inhalation is now recognized as a significant exposure route with measurable consequences for respiratory health.
Polystyrene microplastics induce an immunometabolic active state in macrophages
Researchers investigated how macrophages, the immune cells that act as first-line defense in the gut and lungs, respond metabolically to polystyrene microplastic particles. The study found that phagocytosis of microplastics induced an immunometabolic active state in macrophages, suggesting that microplastic exposure may alter immune cell metabolism in ways relevant to understanding potential health effects.
The Effect of Nanoplastics and Microplastics on Lung Morphology and Physiology: a Systematic Review
This systematic review examines how inhaled microplastics and nanoplastics affect lung structure and function. The research found that indoor microplastic concentrations are often higher than outdoor levels due to household materials shedding fibers, and that inhaled particles can accumulate in different parts of the lungs. These findings suggest that breathing in plastic particles at home and work could contribute to respiratory health problems over time.
Oropharyngeal Administration of Polystyrene Microplastics Induces Profibrotic and Oxidative Changes in Murine Lung Tissue
Researchers investigated the early lung effects of inhaled polystyrene microplastics in mice over a 21-day exposure period. While overall fibrosis scores did not reach statistical significance in this short timeframe, they observed significant macrophage infiltration, active particle uptake by immune cells, and upregulation of oxidative stress and fibrosis-related molecular markers. The findings suggest that microplastic inhalation triggers early immune and oxidative responses that may precede lung tissue remodeling.
Airborne microplastics: A narrative review of potential effects on the human respiratory system
This review consolidates research on airborne microplastics and their potential effects on the human respiratory system. Studies show that inhaled microplastics can deposit in the lungs, trigger inflammation, cause oxidative stress, and lead to cell damage and death. While human exposure evidence is still limited, animal and cell studies suggest that long-term inhalation of airborne microplastics could pose significant risks to lung health.
Potential health risks of the interaction of microplastics and lung surfactant
Researchers investigated how polystyrene microplastics interact with lung surfactant extracted from porcine lungs. The study found that microplastics altered the surface tension and membrane structure of lung surfactant, preferentially adsorbed phospholipid components, and accelerated the production of reactive oxygen species, suggesting potential risks to respiratory health from inhaled microplastics.
Human Exposure to Airborne Microplastics: A Study on Detection and Potential Health Effects Using BAL Fluid
This study detected inhaled microplastics in bronchoalveolar lavage fluid from the lower respiratory tract of human patients and found associations between microplastic presence and markers of lung inflammation and impaired lung function.
Micro- and Nanoplastic-Induced Respiratory Disease and Dysfunction: A Scoping Review
A systematic scoping review of 68 studies found that inhaled micro- and nanoplastics are detected in human lung tissue and associated with pulmonary inflammation, fibrosis, and impaired lung function, though most evidence comes from occupational settings and in vitro experiments.